ymjЯкутский медицинский журналYakut Medical Journal1813-19052312-1017ЯНЦ КМП10.25789/YMJ.2023.83.24ymj-307Research ArticleНАУЧНЫЕ ОБЗОРЫ И ЛЕКЦИИSCIENTIFIC REVIEWS AND LECTURESСовременные представления об апоптозеModern concepts about apoptosisПатракееваВ. П.KontievskayaE. V.

ПАТРАКЕЕВА Вероника Павловна – к.б.н., в.н.с., зав. лаб.

KONTIEVSKAYA Elena Vladimirovna – junior researcher

patrakeewa.veronika@yandex.ruКонтиевскаяЕ. В.PatrakeevaV. P.

КОНТИЕВСКАЯ Елена Владимировна – м.н.с.

PATRAKEEVA Veronika Pavlovna – PhD in Biology, chief researcher, head of the Laboratory of Ecological Immunology

ФИЦ комплексного изучения Арктики им. акад. Н.П. Лаверова УрО РАН, Институт физиологии природных адаптацийРоссияN. Laverov Federal Center for Integrated Arctic Research of the Ural Branch of the Russian Academy of Sciences, Institute of Physiology of Natural AdaptationsRussian Federation2023070220250397101Copyright © Патракеева В.П., Контиевская Е.В., 20252025Патракеева В.П., Контиевская Е.В.Kontievskaya E.V., Patrakeeva V.P.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://ymj.elpub.ru/jour/article/view/307

Обзор посвящен обобщению современных знаний о таком типе клеточной гибели, как апоптоз. На сегодняшний день известно, что апоптоз - это не просто запрограммированная клеточная смерть, обеспечивающая элиминацию старых клеток, происходящая с минимальным повреждением окружающих тканей, но также это сложный механизм, который может способствовать выживанию и пролиферации, а также вызывать и подавлять воспалительный процесс. Активно исследуются препараты, вызывающие усиленный апоптоз, с целью лечения онкологических заболеваний. Механизмы выбора клеточной гибели еще изучаются, но уже известно, что слабые воздействия на макроорганизм способствуют активации апоптоза и аутофагии, а более сильные воздействия – некроз. Низкие уровни апоптоза способствуют накоплению поврежденных клеток, старению и нестабильности генома. Снижение накопления стареющих клеток улучшают гомеостаз и продолжительность жизни.

The review is devoted to the generalization of modern knowledge about such a type of cell death as apoptosis. To date, it is known that apoptosis is not just a programmed cell death that ensures the elimination of old cells with minimal damage to surrounding tissues, but it is also a complex mechanism that can promote survival and proliferation, as well as induce and suppress the inflammatory process. Drugs that cause enhanced apoptosis are being actively studied for the treatment of oncological diseases. The mechanisms of cell death selection are still being studied, but it is already known that weak effects on the macroorganism promote the activation of apoptosis and autophagy, while stronger effects promote necrosis. Low levels of apoptosis contribute to the accumulation of damaged cells, aging, and genome instability. Reduced accumulation of senescent cells improves homeostasis and lifespan.

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The authors declare that there are no conflicts of interest present.